Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain

Shi Ying Huang; Chun Sung Sung; Wu Fu Chen; Chun Hong Chen; Chien Wei Feng; San Nan Yang; Han Chun Hung; Nan Fu Chen; Pey Ru Lin; San Cher Chen; Hui Min David Wang; Tian Huei Chu; Ming Hong Tai; Zhi Hong Wen

doi:10.1186/s12974-015-0280-1

Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain

Shi Ying Huang, Chun Sung Sung, Wu Fu Chen, Chun Hong Chen, Chien Wei Feng, San Nan Yang, Han Chun Hung, Nan Fu Chen, Pey Ru Lin, San Cher Chen, Hui Min David Wang, Tian Huei Chu, Ming Hong Tai, Zhi Hong Wen^*

^*Corresponding author for this work

Research output: Contribution to journal › Journal Article › peer-review

31 Scopus citations

Abstract

Background: Many cancer research studies have extensively examined the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathway. There are only few reports that suggest that PTEN might affect pain; however, there is still a lack of evidence to show the role of PTEN for modulating pain. Here, we report a role for PTEN in a rodent model of neuropathic pain. Results: We found that chronic constriction injury (CCI) surgery in rats could elicit downregulation of spinal PTEN as well as upregulation of phosphorylated PTEN (phospho-PTEN) and phosphorylated mammalian target of rapamycin (phospho-mTOR). After examining such changes in endogenous PTEN in neuropathic rats, we explored the effects of modulating the spinal PTEN pathway on nociceptive behaviors. The normal rats exhibited mechanical allodynia after intrathecal (i.t.) injection of adenovirus-mediated PTEN antisense oligonucleotide (Ad-antisense PTEN). These data indicate the importance of downregulation of spinal PTEN for nociception. Moreover, upregulation of spinal PTEN by i.t. adenovirus-mediated PTEN (Ad-PTEN) significantly prevented CCI-induced development of nociceptive sensitization, thermal hyperalgesia, mechanical allodynia, cold allodynia, and weight-bearing deficits in neuropathic rats. Furthermore, upregulation of spinal PTEN by i.t. Ad-PTEN significantly attenuated CCI-induced microglia and astrocyte activation, upregulation of tumor necrosis factor-α (TNF-α) and phospho-mTOR, and downregulation of PTEN in neuropathic rats 14 days post injury. Conclusions: These findings demonstrate that PTEN plays a key, beneficial role in a rodent model of neuropathic pain.

Original language	English
Article number	59
Journal	Journal of Neuroinflammation
Volume	12
Issue number	1
DOIs	https://doi.org/10.1186/s12974-015-0280-1
State	Published - 26 03 2015
Externally published	Yes

Bibliographical note

Publisher Copyright:
© Huang et al.

Keywords

Astrocyte
Chronic constriction injury
Intrathecal
Neuroinflammation

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1186/s12974-015-0280-1

Cite this

Huang, S. Y., Sung, C. S., Chen, W. F., Chen, C. H., Feng, C. W., Yang, S. N., Hung, H. C., Chen, N. F., Lin, P. R., Chen, S. C., Wang, H. M. D., Chu, T. H., Tai, M. H., & Wen, Z. H. (2015). Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain. Journal of Neuroinflammation, 12(1), Article 59. https://doi.org/10.1186/s12974-015-0280-1

@article{5054f31bd2494b11963cb1f84ed001e0,

title = "Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain",

abstract = "Background: Many cancer research studies have extensively examined the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathway. There are only few reports that suggest that PTEN might affect pain; however, there is still a lack of evidence to show the role of PTEN for modulating pain. Here, we report a role for PTEN in a rodent model of neuropathic pain. Results: We found that chronic constriction injury (CCI) surgery in rats could elicit downregulation of spinal PTEN as well as upregulation of phosphorylated PTEN (phospho-PTEN) and phosphorylated mammalian target of rapamycin (phospho-mTOR). After examining such changes in endogenous PTEN in neuropathic rats, we explored the effects of modulating the spinal PTEN pathway on nociceptive behaviors. The normal rats exhibited mechanical allodynia after intrathecal (i.t.) injection of adenovirus-mediated PTEN antisense oligonucleotide (Ad-antisense PTEN). These data indicate the importance of downregulation of spinal PTEN for nociception. Moreover, upregulation of spinal PTEN by i.t. adenovirus-mediated PTEN (Ad-PTEN) significantly prevented CCI-induced development of nociceptive sensitization, thermal hyperalgesia, mechanical allodynia, cold allodynia, and weight-bearing deficits in neuropathic rats. Furthermore, upregulation of spinal PTEN by i.t. Ad-PTEN significantly attenuated CCI-induced microglia and astrocyte activation, upregulation of tumor necrosis factor-α (TNF-α) and phospho-mTOR, and downregulation of PTEN in neuropathic rats 14 days post injury. Conclusions: These findings demonstrate that PTEN plays a key, beneficial role in a rodent model of neuropathic pain.",

keywords = "Astrocyte, Chronic constriction injury, Intrathecal, Neuroinflammation",

author = "Huang, {Shi Ying} and Sung, {Chun Sung} and Chen, {Wu Fu} and Chen, {Chun Hong} and Feng, {Chien Wei} and Yang, {San Nan} and Hung, {Han Chun} and Chen, {Nan Fu} and Lin, {Pey Ru} and Chen, {San Cher} and Wang, {Hui Min David} and Chu, {Tian Huei} and Tai, {Ming Hong} and Wen, {Zhi Hong}",

note = "Publisher Copyright: {\textcopyright} Huang et al.",

year = "2015",

month = mar,

day = "26",

doi = "10.1186/s12974-015-0280-1",

language = "英语",

volume = "12",

journal = "Journal of Neuroinflammation",

issn = "1742-2094",

publisher = "BioMed Central Ltd",

number = "1",

}

TY - JOUR

T1 - Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain

AU - Huang, Shi Ying

AU - Sung, Chun Sung

AU - Chen, Wu Fu

AU - Chen, Chun Hong

AU - Feng, Chien Wei

AU - Yang, San Nan

AU - Hung, Han Chun

AU - Chen, Nan Fu

AU - Lin, Pey Ru

AU - Chen, San Cher

AU - Wang, Hui Min David

AU - Chu, Tian Huei

AU - Tai, Ming Hong

AU - Wen, Zhi Hong

PY - 2015/3/26

Y1 - 2015/3/26

N2 - Background: Many cancer research studies have extensively examined the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathway. There are only few reports that suggest that PTEN might affect pain; however, there is still a lack of evidence to show the role of PTEN for modulating pain. Here, we report a role for PTEN in a rodent model of neuropathic pain. Results: We found that chronic constriction injury (CCI) surgery in rats could elicit downregulation of spinal PTEN as well as upregulation of phosphorylated PTEN (phospho-PTEN) and phosphorylated mammalian target of rapamycin (phospho-mTOR). After examining such changes in endogenous PTEN in neuropathic rats, we explored the effects of modulating the spinal PTEN pathway on nociceptive behaviors. The normal rats exhibited mechanical allodynia after intrathecal (i.t.) injection of adenovirus-mediated PTEN antisense oligonucleotide (Ad-antisense PTEN). These data indicate the importance of downregulation of spinal PTEN for nociception. Moreover, upregulation of spinal PTEN by i.t. adenovirus-mediated PTEN (Ad-PTEN) significantly prevented CCI-induced development of nociceptive sensitization, thermal hyperalgesia, mechanical allodynia, cold allodynia, and weight-bearing deficits in neuropathic rats. Furthermore, upregulation of spinal PTEN by i.t. Ad-PTEN significantly attenuated CCI-induced microglia and astrocyte activation, upregulation of tumor necrosis factor-α (TNF-α) and phospho-mTOR, and downregulation of PTEN in neuropathic rats 14 days post injury. Conclusions: These findings demonstrate that PTEN plays a key, beneficial role in a rodent model of neuropathic pain.

AB - Background: Many cancer research studies have extensively examined the phosphatase and tensin homolog deleted from chromosome 10 (PTEN) pathway. There are only few reports that suggest that PTEN might affect pain; however, there is still a lack of evidence to show the role of PTEN for modulating pain. Here, we report a role for PTEN in a rodent model of neuropathic pain. Results: We found that chronic constriction injury (CCI) surgery in rats could elicit downregulation of spinal PTEN as well as upregulation of phosphorylated PTEN (phospho-PTEN) and phosphorylated mammalian target of rapamycin (phospho-mTOR). After examining such changes in endogenous PTEN in neuropathic rats, we explored the effects of modulating the spinal PTEN pathway on nociceptive behaviors. The normal rats exhibited mechanical allodynia after intrathecal (i.t.) injection of adenovirus-mediated PTEN antisense oligonucleotide (Ad-antisense PTEN). These data indicate the importance of downregulation of spinal PTEN for nociception. Moreover, upregulation of spinal PTEN by i.t. adenovirus-mediated PTEN (Ad-PTEN) significantly prevented CCI-induced development of nociceptive sensitization, thermal hyperalgesia, mechanical allodynia, cold allodynia, and weight-bearing deficits in neuropathic rats. Furthermore, upregulation of spinal PTEN by i.t. Ad-PTEN significantly attenuated CCI-induced microglia and astrocyte activation, upregulation of tumor necrosis factor-α (TNF-α) and phospho-mTOR, and downregulation of PTEN in neuropathic rats 14 days post injury. Conclusions: These findings demonstrate that PTEN plays a key, beneficial role in a rodent model of neuropathic pain.

KW - Astrocyte

KW - Chronic constriction injury

KW - Intrathecal

KW - Neuroinflammation

UR - http://www.scopus.com/inward/record.url?scp=84926305001&partnerID=8YFLogxK

U2 - 10.1186/s12974-015-0280-1

DO - 10.1186/s12974-015-0280-1

M3 - 文章

C2 - 25889774

AN - SCOPUS:84926305001

SN - 1742-2094

VL - 12

JO - Journal of Neuroinflammation

JF - Journal of Neuroinflammation

IS - 1

M1 - 59

ER -

Involvement of phosphatase and tensin homolog deleted from chromosome 10 in rodent model of neuropathic pain

Abstract

Bibliographical note

Keywords

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this